Comment on: Impact of serum uric acid on renal function after bariatric surgery: a retrospective study

Obesity is an independent risk factor for renal functional decline in people with chronic kidney disease and is highly prevalent among people with the leading cause of chronic kidney disease, diabetic kidney disease [1]. Intentional weight loss strategies hold promise as a means of arresting progressive renal functional decline in diabetic kidney disease [2]. Optimization of renal outcomes after metabolic surgery centers on blood pressure and glycemic control, as well as addressing proteinuria. The role of uric acid–lowering in this setting is controversial. Purines (adenine, guanine) from nucleic acids (RNA, DNA) are metabolized to xanthine and hypoxanthine, and subsequently converted to uric acid by xanthine oxidase [3]. Uric acid is a nitrogenous waste product, which is excreted via the urine. Epidemiologic studies highlight a relationship between hyperuricemia and renal functional decline, proteinuria, and cardiovascular disease [4]. Whether serum uric acid plays a causal role in chronic kidney disease progression or is simply a biomarker of kidney function remains a controversial question, which is currently being addressed by placebo-controlled, randomized controlled studies, such as the PERL study in which people with diabetic kidney disease and hyperuricemia are randomized to uric acid–lowering therapy or placebo [5]. The present study by Hung et al. [6] adds to the observational evidence implicating uric acid as a marker of adverse renal outcomes and, importantly, is the first study to examine this phenomenon in patients with and without baseline chronic kidney disease after metabolic surgery.